A stroke, or cerebrovascular accident (CVA), is the rapid loss of brain function due to disturbance in the blood supply to the brain. This can be due to ischemia (lack of blood flow) caused by blockage (thrombosis, arterial embolism), or a hemorrhage (broadly termed “neurological insult”). As a result, and often worsening over time, brain injury becomes permanent dysfunction/damage. Typically, affected areas of the brain have diminished or complete loss of function. In particular instances this is exhibited as an inability or reduced ability to move one or more limbs on one side of the body, inability to or difficulty in understanding or formulating speech, or an inability to see one side of the visual field. In the case of stroke, secondary neuronal damage following the initial insult is a significant factor in patient decline and eventual death. This decline manifests itself weeks to months following the initial stoke and, without effective therapeutic intervention, leads to a slow but continuous decline in the patients physical and mental health.
In the case of TBI, the progression of damage is typically slower than that in stroke. Recent reports, however, establish TBI as equally destructive in outcome in the more severe cases Current reports find that about 40% of people with TBI exhibit a continuing decline in both physical and mental capacity. This represents a significantly higher incidence of dementia, in some instances is an aggravating factor in death.
An important consideration in therapeutic treatment and improved outcomes in patients afflicted with neuronal injury (including either Stroke or TBI) is to block secondary injury of surrounding neurons that were not, in the first instance, directly affected by the primary insult. Literature reports that secondary neuronal damage occurs after a variety of brain insults including subarachnoid hemorrhage, stroke, and traumatic brain injury and involves metabolic cascades. Noted metabolic aspects include prolonged secondary ischemia, cerebral hypoxia, hypotension, cerebral edema, changes in the blood flow to the brain; and raised intracranial pressure. Other secondary insults include hypercapnia, acidosis, meningitis, and brain abscess. In addition, alterations in the release of neurotransmitters particularly glutamate can cause excitotoxic neuronal cell death by causing free radicals generation and oxidative stress within these neurons that leads to neurodegeneration.
The following references are noted, the teachings of which are incorporated by reference in their entirety:
1. The Behavioral and Cognitive Neurology of Stroke Ed. Olivier Godefroy (Cambridge University Press, 2nd edition, 2013);
2. Stroke Rehabilitation: A Function-Based Approach, 3rd, Ed. Glen Gilled, (Mosby, 2010);
3. Stroke Part III: Investigation and management, Volume 94: Handbook of Clinical Neurology (Series Editors: Aminoff, Boller and Swaab, Ed. Marc Fisher (Elsiver 2009);
4. Traumatic Brain Injury: Methods for Clinical and Forensic Neuropsychiatric Assessment, Second Edition, Robert P. Granacher Jr. (CRC Press 2007);
5. Sports Neuropsychology: Assessment and Management of Traumatic Brain Injury, Ed. Ruben J. Echemendia PhD (The Guilford Press, 2006);
6. Brain Injury Medicine: Principles and Practice, Second Edition Ed. Nathan D. Zasler MD (Demos Medical; 2012); and
7. Blockade of PARP activity attenuates poly(ADP-ribosyl)ation but offers only partial neuroprotection against NMDA-induced cell death in the rat retina. (Goebel and Winkler, J Neuro Chem, 98:1732-1745, 2006) (NMDA-induced chemical stroke in vivo rat retinal neurotoxicity model).
Reference is made to the Glasgow Coma Scale. The Glasgow Coma Scale 15-point test used to assess the initial severity of a brain injury by checking a person's ability to follow directions and move their eyes and limbs. Abilities are scored numerically. Higher scores mean milder injuries.